DNA Damage News and Research

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Research finding suggests HCV interference with hepcidin synthesis

Iron overload, a common feature of chronic liver disorders, has been linked with oxidative DNA damage, insulin resistance and liver steatosis, and with triggering of hepatic stellate cells thus inducing liver fibrosis.

13 Apr 2010

Ku protein employs unique mechanism for DNA repair: Researchers

Scientists have shown in multiple contexts that DNA damage over our lifetimes is a key mechanism behind the development of cancer and other age-related diseases. Not everyone gets these diseases, because the body has multiple mechanisms for repairing the damage caused to DNA by aging, the environment and other human behaviors - but the mechanisms behind certain kinds of DNA repair have not been well-understood.

12 Apr 2010

Recql5 identified as a tumor suppressor in GI tract

Recql5 is a member of the mammalian RecQ helicase family. Genetic mutations that result in loss of RecQ helicase activity give rise to disorders that are associated with cancer predisposition and premature aging, such as Bloom, Werner, and Rothmund-Thomson syndromes. This class of enzymes is best known for their role in maintaining the integrity of the genome to prevent oncogenic mutations.

9 Apr 2010

Blocking POLQ gene activity can increase ability of radiotherapy to destroy tumours

Cancer Research UK scientists have identified a gene that once blocked could increase the effectiveness of radiotherapy on tumours, according to research published in Cancer Research today (Thursday).

7 Apr 2010

New production method yields hundredsfold more ubiquitylated proteins critical for cancer research

Scientists at the University of Delaware have developed a new method for producing proteins critical to research on cancer, Alzheimer's, and other diseases.

3 Apr 2010

New insights on events that lead to immortalized cells

Researchers at Umeå University can now show that cells that grow forever get this capacity through gradual changes in the expression of genes that govern the repair of DNA damage and regulate growth and cell death. The research also shows that activation of the enzyme complex telomerase, which is necessary for unlimited growth, occurs late in this process.

29 Mar 2010

Genetic instability in people with Fanconi anemia: New proteins in FA DNA repair pathway may help explain

Identification of two new proteins in the Fanconi anemia DNA repair pathway may help explain genetic instability in people with Fanconi anemia and how otherwise healthy people are susceptible to cancer from environmentally triggered DNA damage.

26 Mar 2010

Novel ways of killing TB causing bacteria discovered

Researchers at Albert Einstein College of Medicine of Yeshiva University have found two novel ways of killing the bacteria that cause tuberculosis (TB), a disease responsible for an estimated two million deaths each year. The findings, published in the March 21 online issue of Nature Chemical Biology, could lead to a potent TB therapy that would also prevent resistant TB strains from developing.

22 Mar 2010

Breast cancer survivors at increased risk of developing second cancer: Study

Certain rare mutations in the ataxia telangiectasia mutated gene, combined with radiation exposure, may increase a woman's risk of developing a second cancer in the opposite breast, according to a study published online March 19 in the Journal of the National Cancer Institute.

20 Mar 2010

Nanobotmodels Company offer vision of future DNA and cell-repair techniques

Developments in nanotechnology and nanorobotics are opening up the prospects for nanomedicine and regenerative medicine where informatics and DNA computing can become the catalysts enabling health care applications at sub-molecular or atomic scales. While nanomedicine promises a new exciting frontier for clinical practice and biomedical research, issues involving cost-effectiveness studies, clinical trials and toxicity assays, drug delivery methods, and the implementation of new personalized therapies still remain challenging.

18 Mar 2010

Novel findings point to new therapeutic approaches for common types of cancer

Increased understanding of the Skp2 gene and its relation to cellular senescence may lead to the development of novel agents that can suppress tumor development in common types of cancer, researchers from The University of Texas M. D. Anderson Cancer Center and Memorial Sloan-Kettering Cancer Center report in the journal Nature.

18 Mar 2010

Gene defects could become targets for new personalised treatments for bowel cancer

Cancer Research UK-funded scientists have discovered that the gene defects that cause some bowel cancers could become the targets for new personalised treatments. Their research is published in Cancer Cell today (Monday).

16 Mar 2010

ES cells-functions: Condensins promote mitotic progression and maintain interphase chromatin compaction

Regulatory proteins common to all eukaryotic cells can have additional, unique functions in embryonic stem (ES) cells, according to a study in the February 22 issue of the Journal of Cell Biology (www.jcb.org). If cancer progenitor cells-which function similarly to stem cells-are shown to rely on these regulatory proteins in the same way, it may be possible to target them therapeutically without harming healthy neighboring cells.

24 Feb 2010

ATM tumor-suppressor also recognizes damage caused by ROS and orders autophagy

ATM, a protein that reacts to DNA damage by ordering repairs or the suicide of the defective cell, plays a similar, previously unknown role in response to oxidative damage outside of the nucleus, researchers report this week in the online version of the Proceedings of the National Academy of Sciences.

19 Feb 2010

Roche Molecular Systems, Merck Sharp & Dohme announce cancer therapeutics collaboration

Roche Molecular Systems, Inc. announced today a research collaboration with Merck Sharp & Dohme Corp. (a subsidiary of Merck & Co., Inc.) providing Merck access to Roche's developmental microarray-based AmpliChip p53 Test, which is designed to detect mutations in the tumor suppressor gene p53. By identifying cancers that harbor a dysfunctional p53 gene, the companies aim to achieve better treatment outcomes in cancer patients by determining which patients are most likely to respond to certain investigational therapeutic candidates.

18 Feb 2010

Treating bacteria with insufficient levels of antibiotics leads to multidrug resistance in 'superbugs'

For years, doctors have warned patients to finish their antibiotic prescriptions or risk a renewed infection by a "superbug" that can mount a more powerful defense against the same drug. But a new study by Boston University biomedical engineers indicates that treating bacteria with levels of antibiotics insufficient to kill them produces germs that are cross-resistant to a wide range of antibiotics.

12 Feb 2010

Research suggests a potential means of circumventing drug resistance in breast cancer patients

Overexpression of low-molecular-weight (LMW-E) forms of the protein cyclin E renders the aromatase inhibitor letrozole ineffective among women with estrogen-receptor-positive (ER+) breast cancers, researchers from The University of Texas M. D. Anderson Cancer Center report in Clinical Cancer Research.

10 Feb 2010

Study: New mechanism may allow bacteria to develop resistance to antibiotics

Scientists have shown that cells' DNA-reading machinery can skim through certain kinds of damaged DNA without skipping any letters in the genetic "text." The studies, performed in bacteria, suggest a new mechanism that can allow bacteria to develop resistance to antibiotics.

10 Feb 2010

Boston researchers identify new mechanism that inhibit tumor growth in mice

A team of researchers, led by Pier Paolo Pandolfi, at Beth Israel Deaconess Medical Center, Boston, has identified a new type of cellular senescence (i.e., irreversible arrest of cell growth) and determined a way to enhance it to suppress prostate tumor development and growth in mice.

9 Feb 2010

Researchers explain how HSV dismantles host's defense systems

A viral infection is like an uninvited, tenacious houseguest in the cell, using a range of tricks to prevent its eviction. Researchers at the Salk Institute for Biological Studies have identified one of the key proteins allowing herpes simplex virus (HSV) DNA to fly under the radar of their hosts' involuntary hospitality.

21 Jan 2010